Chlamydia trachomatis is responsible for more than 1.4 million genital infections in the United States annually, making it the most prevalent bacterial sexually transmitted infection (STI). However, the vast majority of these infections are asymptomatic, demonstrating the need for the development of a preventative vaccine. A vaccine recapitulating in humans the humoral immunity seen in the highly related Chlamydia muridarum murine model of genital infection, which exhibits marked antibody-mediated protection to reinfection, could be highly efficacious. Our results have demonstrated a prominent role for the potent activating cytokine gamma interferon (IFN-γ) in humoral protection. The function of IFN-γ in humoral immunity to chlamydial genital infection is effector cell activation, and is independent of antibody class switching. Additionally, we identified neutrophils as a key effector cell population contributing to antibody-mediated immunity. Conversely, NK cells, which represent another cell population capable of functioning with antibody in protective immunity, were found to be dispensable for humoral protection against genital chlamydia. These data collectively highlight the requirement of antibody/effector cell interactions in mediating humoral protection against genital chlamydia, and should prove important in future considerations regarding activation of specific populations during vaccine development.
|Advisor:||Morrison, Richard P.|
|Commitee:||Diekman, Alan, Gilbert, Kathleen, Stumhofer, Jason, Voth, Daniel|
|School:||University of Arkansas for Medical Sciences|
|Department:||Microbiology and Immunology|
|School Location:||United States -- Arkansas|
|Source:||DAI-B 79/04(E), Dissertation Abstracts International|
|Keywords:||Effectors, Elucidating immune mediators, Genital Chlamydia, Humoral protection|
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